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Aegle marmelos fruit extract abates dextran sodium sulfate induced acute colitis in mice: Repression of pro-inflammatory cytokines during colonic inflammation

机译:Aegle marmelos水果提取物可减轻右旋糖酐硫酸钠诱发的小鼠急性结肠炎:结肠炎症过程中促炎性细胞因子的抑制

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摘要

Ulcerative colitis (UC) is a common inflammatory bowel disease which on prolongation causes colorectal cancer (CRC) making UC as the highest risk factor for CRC development. Despite the use of Aegle marmelos in folk medicine, few studies have reported its colonic healing activity. We exploited the use of dextran sodium sulfate (DSS) in inducing colitis in Swiss albino mice and examine the inflammatory modulating effect of A. marmelos fruit extract (AME). HPLC analysis confirmed the presence of two biologically active compounds namely umbelliferon (a coumarin-derivative) and lupeol (triterpenoid). Fourteen days feeding of DSS to mice elicited colitis, with drastically reduced body weight with altered clinical severity score, combined with shortening of colon length. Oral administration of AME (50. mg/kg) evidenced a significant suppression of disease symptoms. The increased mRNA expressions of interleukin (IL) 2, IL-6 and tumor necrosis factor α during colitis, were also reduced significantly. Notable reduction in the NF-κB expression in the colonic region was also noted which is substantiates with docking analysis were UMB and LUP found in AME bounds with NF-κB. Furthermore, DSS-altered histopathological features of colon were also recovered on treatment with AME. Thus the observation revealed the restorative significance of AME in healing the DSS-induced colitis in mice by modulating NF-κB and regulating pro-inflammatory mediators involved in the colonic injury.
机译:溃疡性结肠炎(UC)是一种常见的炎症性肠病,延长病程会导致结直肠癌(CRC),从而使UC成为CRC发展的最高风险因素。尽管在民间医学中使用了Aegle marmelos,但很少有研究报道其结肠愈合活性。我们利用右旋糖酐硫酸钠(DSS)诱导瑞士白化病小鼠结肠炎,并研究了A. marmelos水果提取物(AME)的炎症调节作用。 HPLC分析证实存在两种生物活性化合物,即伞形酮(香豆素衍生物)和羽扇豆油(三萜)。将DSS喂给小鼠十四天会引起结肠炎,体重急剧下降,临床严重性评分改变,同时结肠长度缩短。口服AME(50. mg / kg)证明可以明显抑制疾病症状。结肠炎期间白介素(IL)2,IL-6和肿瘤坏死因子α的mRNA表达增加也明显降低。还注意到结肠区域中NF-κB表达的显着降低,这是通过对接分析证实的,即在AME与NF-κB的结合中发现了UMB和LUP。此外,在用AME治疗后,还恢复了DSS改变的结肠组织病理学特征。因此,该观察结果揭示了AME通过调节NF-κB和调节参与结肠损伤的促炎性介质,在治愈DSS诱导的小鼠结肠炎中具有恢复性意义。

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